ArticleJournal of virology2006
ORF66 protein kinase function is required for T-cell tropism of varicella-zoster virus in vivo.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- Herpes Zoster: Risk Factors for Occurrence, Complications, and Recurrence with a Focus on Immunocompromised Patients.Diseases (Basel, Switzerland) · 2025Review
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Mouse Models for Human Herpesviruses.Pathogens (Basel, Switzerland) · 2023Review
- Insights From Studies of the Genetics, Pathogenesis, and Immunogenicity of the Varicella Vaccine.The Journal of infectious diseases · 2022Article
- Insights into the pathogenesis of varicella viruses.Current clinical microbiology reports · 2019Article
- Varicella-Zoster Virus ORF63 Protects Human Neuronal and Keratinocyte Cell Lines from Apoptosis and Changes Its Localization upon Apoptosis Induction.Journal of virology · 2018Article
- Sex differences underlying orofacial varicella zoster associated pain in rats.BMC neurology · 2017Article
- Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration.PLoS pathogens · 2017Article
- Role for the Ventral Posterior Medial/Posterior Lateral Thalamus and Anterior Cingulate Cortex in Affective/Motivation Pain Induced by Varicella Zoster Virus.Frontiers in integrative neuroscience · 2017Article
- Varicella-Zoster Virus Activates CREB, and Inhibition of the pCREB-p300/CBP Interaction Inhibits Viral Replication In Vitro and Skin Pathogenesis In Vivo.Journal of virology · 2016Article
- Dissecting the Molecular Mechanisms of the Tropism of Varicella-Zoster Virus for Human T Cells.Journal of virology · 2016Review
- Infected peripheral blood mononuclear cells transmit latent varicella zoster virus infection to the guinea pig enteric nervous system.Journal of neurovirology · 2014Article
- Molecular mechanisms of varicella zoster virus pathogenesis.Nature reviews. Microbiology · 2014Review
- Age and immune status of rhesus macaques impact simian varicella virus gene expression in sensory ganglia.Journal of virology · 2013Article
- Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in immunodeficient hosts.PLoS pathogens · 2012Article
- The alphaherpesvirus US3/ORF66 protein kinases direct phosphorylation of the nuclear matrix protein matrin 3.Journal of virology · 2011Article
- Hyperphosphorylation of histone deacetylase 2 by alphaherpesvirus US3 kinases.Journal of virology · 2010Article
- Varicella-zoster virus open reading frame 66 protein kinase and its relationship to alphaherpesvirus US3 kinases.Current topics in microbiology and immunology · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Several functions have been attributed to the serine/threonine protein kinase encoded by open reading frame 66 (ORF66) of varicella-zoster virus (VZV), including modulation of the apoptosis and interferon pathways, down-regulation of major histocompatibility complex class I cell surface expression, and regulation of IE62 localization. The amino acid sequence of the ORF66 protein contains a recognizable conserved kinase domain. Point mutations were introduced into conserved protein kinase motifs to evaluate their importance to ORF66 protein functions. Two substitution mutants were generated, including a G102A substitution, which blocked autophosphorylation and altered IE62 localization, and an S250P substitution, which had no effect on either autophosphorylation or IE62 localization. Both kinase domain mutants grew to titers equivalent to recombinant parent Oka (pOka) in vitro. pOka66G102A had slightly reduced growth in skin, which was comparable to the reduction observed when ORF66 translation was prevented by stop codon insertions in pOka66S. In contrast, infection of T-cell xenografts with pOka66G102A was associated with a significant decrease in infectious virus production equivalent to the impaired T-cell tropism found with pOka66S infection of T-cell xenografts in vivo. Disrupting kinase activity with the G102A mutation did not alter IE62 cytoplasmic localization in VZV-infected T cells, suggesting that decreased T-cell tropism is due to other ORF66 protein functions. The G102A mutation reduced the antiapoptotic effects of VZV infection of T cells. These experiments indicate that the T-cell tropism of VZV depends upon intact ORF66 protein kinase function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.